2- Substance misuse Flashcards

1
Q

Acute intoxication:

A

The acute, usually transient, effect of the substance.

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2
Q

Harmful use:

A

Recurrent misuse associated with physical, psychological and social consequences, but without dependence.

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3
Q

Dependence syndrome:

A

Prolonged, compulsive substance use leading to addiction, tolerance and the potential for withdrawal syndromes.

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4
Q

Withdrawal state:

A

Physical and/or psychological effects from complete (or partial) cessation of a substance after prolonged, repeated or high level of use.

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5
Q

Psychotic disorder:

A

Onset of psychotic symptoms within 2 weeks of substance use. Must persist for more than 48 hours.

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6
Q

Amnesic syndrome:

A

Memory impairment in recent memory (impaired learning of new material) and ability to recall past experiences. Also defect in recall, clouding of consciousness and global intellectual decline.

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7
Q

Residual disorder:

A

Specific features (flashbacks, personality disorder, affective disorder, dementia, persisting cognitive impairment) subsequent to substance misuse.

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8
Q

prevalence of substance misuse

A

M?F 3:1
- Cannabis most commonly consumed drug, used by 5% of the population

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9
Q

pathophysiology of substance misuses

A
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10
Q

Classes of drugs

A
  • Opiates
  • Cannabinoids
  • Sedatives- hypnotics
  • Stimulants
  • Hallucinogens
  • Anabolic steroids
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11
Q

complications of substance misuse

A
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12
Q

Substance misuse presentation with acronynm

A

DRUG PROBLEMS WILL CONTUNUE TO HARM >3 of the following manifestations

  • (1) Strong Desire (compulsion) to consume substance;
  • (2) Preoccupation with substance use.
  • (3) Withdrawal state when substance ingestion is reduced or stopped;
  • (4) Impaired ability to Control substance-taking behaviour (e.g. onset, termination or level of use);
  • (5) Tolerance to substance, requiring more consumption for desired effect;
  • (6) Persisting with use, despite clear evidence to the Harmful effects.
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13
Q

examples of opiates

A

e.g. morphine, diamorphine (heroin), codeine, methadone

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14
Q

routes of opiates

A
  • Morphine- PO,IV
  • Diamorphine – IN, IV, smoked
  • Codeine/ methadone -PO
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15
Q

effects of opiates

A

1) Psychological
Apathy, disinhibition, psychomotor retardation, impaired judgement and attention, drowsiness, slurred speech

2) Physical
Respiratory depression, hypoxia, decreased BP, hypothermia, coma, pupillary constriction

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16
Q

withdrawal state of opiates

A

Withdrawal states (at least 3 signs needed)
Craving, rhinorrhoea, lacrimation, myalgia, abdominal cramps, N+V, diarrhoea, pupillary dilatation, piloerection, increased HR/ BP

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17
Q

Management of opioid dependence

A
  • First line: methadone
  • Or buprenorphine for detox and maintenance
  • Naltrexone (recommended for those who were formerly opioid-dependent but have now stopped and are motivated)
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18
Q

Management of opioid overdose

A
  • Intravenous naloxone (antidote)
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19
Q

overdose

A
  • Growing problem
  • Large number of iatrogenic addicts
  • 1 in 4 will develop addiction
  • 9.6% rise in drug related deaths 20162017
  • 67.8% caused by opiates
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20
Q

how is opiate overdose mediated

A
  • U (MOP) receptor
  • As you take more and more you need to take more to get relief
  • Variable effects of doses
  • Main cause of death is resp depression- acidosis
  • Naloxone= treatment
  • Be a vigilant prescriber
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21
Q

cannabinoids example

A

cannabis

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22
Q

route of cannabinoids

A

PO or smoke

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23
Q

effects of cannabinoids

A

1) Psychological
Euphoria, disinhibition, agitation, paranoid ideation, temporal slowing (time passes slowly), impaired judgement/ attention/reaction time, illusions, hallucinations

2) Physical
Increased appetite, dry mouth, conjunctival injection, increased HR

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24
Q

withdrawal state of cannabinous

A

Withdrawal state (at least 3 signs needed)
Anxiety, irritability, tremor of outstretched hands, sweating, myalgia

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25
Q

sedative hypnotics examples

A

e.g. benzodiazepines,
barbiturates

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26
Q

route of sedtive hypnotics

A
  • PO, IV
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27
Q

effects of sedative hypnotics

A

Effects
1) Psychological
Euphoria, disinhibition, apathy, aggression, anterograde amnesia, labile mood

2) Physical
Unsteady gait, difficulty standing, slurred speech, nystagmus, erythematous skin lesions, decreased BP, hypothermia, depression of gag reflex, coma

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28
Q

withdrawal state of sedative hypnotics

A

Withdrawal state (at least 3 signs needed)
Tremor of hands, tongue or eyelids, N+V, increased HR, postural
decreased BP, headache, agitation, malaise, transient illusions/ hallucinations, paranoid ideation, grand mal convulsions

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29
Q

example of stimulatants

A

e.g. cocaine, crack cocaine, ecstasy (MDMA), amphetamine

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30
Q

route of stimulants

A
  • Cocaine and crack (IN, IV, smoked)
  • Ecstasy (PO)
  • Amphetamine (PO, IV, IN, smoked)
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31
Q

effects of stimulants

A

Effects
1) Psychological
Euphoria, increased energy, grandiose beliefs, aggression, argumentative, illusions, hallucinations (intact orientation), paranoid ideation, labile mood
2) Physical
Increased HR and BP, arrhythmias, sweating, N+V, pupillary dilatation, psychomotor agitation, muscular weakness, chest pain, convulsions

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32
Q

withdrawal state of stimulants

A

Dysphoric mood (must
be present), lethargy, psychomotor agitation, craving, increased appetite, insomnia (or hypersomnia), bizarre/unpleasant dreams

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33
Q

exampke hallucinogens

A

Hallucinogens
e.g. LSD (lysergic acid diethylamide), magic mushrooms

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34
Q

route of hallucinogens

A

PO

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35
Q

effects of hallucinogens

A

Effects
1) Psychological
Anxiety, illusions, hallucinations, depersonalization, derealization, paranoia, ideas of reference, hyperactivity, impulsivity, inattention
2) Physical
Increased HR, palpitations, sweating, tremor, blurred vision, pupillary dilatation, incoordination

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36
Q

withdrawal state of hallucinogens

A

n/a

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37
Q

example volatile solvents

A

e.g. aerosols, paint, glue, petrol

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38
Q

route volatile solvents

A

inhaled

39
Q

effects of volatile solvents

A

Effects
1) Psychological
Apathy, lethargy, aggression, impaired attention and judgement, psychomotor retardation

2) Physical
Unsteady gait, diplopia, nystagmus, decreased consciousness, muscle weakness

40
Q

withdrawal state of volatile solvents

A

n/a

41
Q

examples of anabolics

A

e.g. testosterone, androstenedione, danazol

42
Q

route of anabolics

A
  • PO, IM
43
Q

effects of anabolics

A

Effects
1) Psychological
Euphoria, depression, aggression, hyperactivity, mood swings, hallucinations, delusions

2) Physical
Increased muscle mass, reduced fat, acne, male pattern baldness, reduced sperm count/infertility, stunted growth

44
Q

withdrawal state of anabolic steroids

A

n/a

45
Q

diagnosis/investigation for drug misuse

A

1) History
2) MSE
3) Risk assessment
4) Investigations

46
Q

history for drug misuse

A
  • ‘Have you ever taken any recreational drugs? If so, how often do you take them, and for how long have you done this?’, ‘How much money do you spend, per week, on drugs?’ (quantity)
  • ‘What are the effects when you take the drug?’ (drug effects)
  • ‘What impact has the drug had on your life?’ (occupation, relationships, forensic history)
  • ‘Do you feel that taking the drug is always at the forefront of your mind?’ (preoccupation)
  • ‘Have you ever tried reducing the substance you’re taking? Any problems with this?’ (withdrawal)
  • ‘Are you able to control your consumption?’ (control)
  • ‘Do you recently feel that you have to take more of the drug to get the same effect?’ (tolerance)
  • ‘Are you aware of the harmful effects?’ (knowledge of harm)
47
Q

MSE for drug misuse

A
48
Q

risk assessment for drug misuse

A
  • BBV
  • Suicide/ self-harm
  • Hurting others
49
Q

investigations for drug misuse

A
  • Bloods
    o HHV screen: HIV, HepB, HepC and TB testing
    o U&Es, LFTs, clotting
    o Drug levels
  • Urinalysis (drug metabolites e.g. cannabis, opioids) can be detected
  • ECG for arrhythmia
  • ECHO for endocarditis (needle sharing)
50
Q

DD for drug misuse

A
  • Psychosis
  • Mood disorders
  • Anxiety
  • Delirium
  • Hyperthyroidism
  • CVA
  • Intracranial haemorrhage
51
Q

general management of drug misuse

A

bio psycho social

52
Q

biological management of drug misuse

A

o Hep B immunisation
o Therapies if relevant
o Help with co-existing alcohol misuse and smoking cessation

53
Q

psychological management of drug misuse

A

o Motivational interviewing
o CBT
o Contingency management
 A technique that focuses on changing specified behaviours by offering incentives e.g. financial for positive behaviours such as abstinence

54
Q

social management of drug misuse

A

o Supportive help: housing, finance, employment
o Self help groups e.g. narcotic anonymous and cocaine anonymous
o Consider issue of driving

55
Q

drugs used to treat / manage opioid addiction /overdose

A

First line: methadone
Second line: buprenorphine
Overdose: naloxone

55
Q

drugs used to stop opioids

A

methadone

56
Q

buprenorphine drug class

A

Mixed agonist- antagonist

57
Q

uses of buprenorphine

A
  • Moderate- severe pain
  • Opioid addiction treatment
58
Q

uses of buprenorphine

A
  • Moderate- severe pain
  • Opioid addiction treatment
59
Q

MOA of buprenorphine

A
  • Partial agonists to mu (MOP) receptor, meaning it only partially activates opiate receptors
  • Also weak kapp receptor antagonist and delta receptor agonists
  • Compared to morphine:
    o Very high affinity for μ receptor
    o Low Kd
    o Long duration of action
    o Not easily displaced
     Difficult to reverse effect
    o Lower E(max) as partial agonist, lower efficacy  less side effect
  • Antagonistic κ receptors
60
Q

ADR buprenorphine

A
  • Respiratory depression
  • Low BP
  • Nausea
  • Dizziness
61
Q

contraindication of buprenorphine

A
  • Hepatitis
  • Liver problems
  • Alcohol intoxication
  • Biliary and gall bladder problems
62
Q

drug drug interaction buprenorphine

A
  • Amiodarone
  • amlodipine
63
Q

naloxone drug class

A

Opioid antagonist

64
Q

uses of nalaoxone

A
  • Rapidly reverse opioid overdose
65
Q

MOA of naloxone

A
  • Competitive antagonism of opioid – MU or MOP receptor
  • Blocks effect of other opioids e.g. morphine
  • Therefore increase in cAMP, increase pain, less of a high
66
Q

ADR of naloxone

A

short half life
o Must give as slow infusion (gradual displacement of morphine)
o If given in a rapid bolus will rapidly wear off the effect of morphine, however then the effects of morphine may become toxic again rapidly because its not been metabolised/excreted yet

67
Q

contraindication of naloxone

A
  • Pts known to be hypersensitive
  • Cardiac problems- caution
68
Q

DDI naloxone

A
  • Codeine
  • Tramadol
  • Opium
  • Morphine (good)
69
Q

Alcohol abuse

A

is the consumption of alcohol at a level sufficient to cause physical, psychiatric and/or social harm.

70
Q

Binge drinking

A

is drinking over twice the recommended level of alcohol per day, in one session (>8 units for males and >6 units for females).

71
Q

Harmful alcohol

A

use is defined as drinking above safe levels with evidence of alcohol-related problems (>50 units/week for men and >35 units/week for females).

72
Q

recommendation for maximum alcohol

A

14 units

73
Q

recommendation for maximum alcohol

A
74
Q

prevalence of alcohol abuse

A
  • Roughly 25% of males and 15% of females drink over the recommended level in the UK.
  • Alcohol dependence affects 4% of people between the ages of 16 and 65 in England.
75
Q

RF for alcoholism

A
  • Males
  • Younger adults
  • Genetics e.g. monozygotic twins have higher concordance than dizygotic
  • Antisocial behaviours
  • Lack of facial flushing e.g. lack of aldehyde dehydrogenase
  • Life stressors e.g. financial problems, marital status
76
Q

neurological pathophysiology of alcohol abuse

A
  • Alcohol affects several neurotransmitter systems in the brain (e.g. its effect on GABA causes anxiolytic and sedative effects).
  • The pleasurable and stimulant effects of alcohol are mediated by a dopaminergic pathway in the brain. Repeated, excessive alcohol ingestion sensitizes this pathway and leads to the development of dependence.
  • Long-term exposure to alcohol causes adaptive
    changes in several neurotransmitter systems,
    including down-regulation of inhibitory
    neuronal GABA receptors and up-regulation of excitatory glutamate receptors, so when alcohol is withdrawn, it results in central nervous system hyper-excitability.
  • Patients with alcohol-use disorders often experience craving (a conscious desire or urge to drink alcohol). This has been linked to dopaminergic, serotonergic, and opioid systems that mediate positive reinforcement, and to the GABA, glutamatergic, and noradrenergic systems that mediate withdrawal.
77
Q

psychological theories of pathophysiology

A

1) The social learning theory suggests that drinking behaviour is modelled on imitation of relatives or friends.
2) Operant conditioning states that positive or negative reinforcement from the effects of drinking will either perpetuate or deter drinking habits, respectively.

78
Q

presentation of intoxification

A
  • Slurred speech
  • Labile affect
  • Impaired judgement
  • Poor co-ordination
  • In severe cases
    o Hypoglycaemia
    o Stupor
    o Coma
79
Q

presentation of dependence

A
  • Subjective awareness of compulsion to drink.
  • Avoidance or relief of withdrawal symptoms by further drinking (also known as relief drinking).
  • Withdrawal symptoms.
  • Drink-seeking behaviour predominates.
  • Reinstatement of drinking after attempted abstinence.
  • Increased tolerance to alcohol.
  • Narrowing of drinking repertoire
    (i.e. a stereotyped pattern of drinking – individuals have fixed as opposed to variable times for drinking, with reduced influence from environmental cues) – only drink same drink e.g. cheap cider
80
Q

sign of alcohol abuse

A
81
Q

presenation of withdrawl of alcohol

A
  • Malaise
  • Tremor
  • Nausea
  • Insomnia
  • Transient hallucinations
  • Autonomic hyperactivity (6-12 hours after abstinence)
  • Seizures (peak incidence at 36 hours)
  • Delirium tremens – peak at 72 hours
82
Q

delirium tremens

A
83
Q

ICD-10 criteria for alcohol abuse

A
84
Q

bio-psychosocial management of alcohol abuse

A
85
Q

management of alcohol withdrawal

A

Alcohol withdrawal
- Alcohol detoxification regime
- High dose benzodiazepines (commonly chlordiazepoxide), are given initially, and the dose is tapered down over 5-9 days
- Thiamines (Vit B1) to prevent Wernickes encephalopathy
o Orally or IV as Pabrinex

86
Q

management of alcohol dependence (long term): biological

A
  • Disulfiram: Works by causing a build-up of acetaldehyde on consumption of alcohol, causing unpleasant symptoms e.g. anxiety, flushing and headache.
  • Acamprosate: Reduces craving by enhancing GABA transmission.
  • Naltrexone: Blocks opioid receptors (antagonist) in
    the body, thus reducing the pleasurable effects of alcohol.
87
Q

management of alcohol dependence : psychological

A

o Motivational interviewing
o CBT

88
Q

management of alcohol dependence : social

A

Alcoholics anonymous- 12 step approach

89
Q

diagnosis / investigation for alcohol abuse

A

1) History/ questionnaires
2) Risk assessment
3) Investigations

90
Q

questionnaire for alcohol abuse

A

CAGE

91
Q

history for alcohol abuse

A

Establish drinking pattern and quantity consumed
* ‘Can you describe what drinks you have in a typical day?’
* ‘How much alcohol do you consume in an average week?’ (quantify number of units)
* ‘How much money do you spend on drinking?’
* ‘How often do you consume alcohol?’
* ‘Do you drink steadily or have periods of binge drinking?’
* ‘Is there anything in particular which causes you to drink more?’
Explore features of alcohol dependence
* ‘When and where do you normally drink?’ (narrowing of drinking repertoire)
* ‘Do you often feel the urge to drink?’ (compulsive need to drink)
* ‘Have you noticed that alcohol has less effect on you than it had in the past?’ (􏰁 tolerance)
* ‘Is alcohol the first thing that comes into your mind when planning a social gathering?’
(drink-seeking behaviour predominates)
* ‘Do you ever feel shaky and anxious when you haven’t had a drink?’, ‘Have you ever tried to give up drinking, if so what happened?’ (withdrawal effects)
* ‘Do you ever drink to get rid of this feeling?’ (prevention of withdrawal effects)
Explore possible risk factors
* ‘Is there any family history of alcohol-related problems?’
* Explore other risk factors, e.g. financial difficulties, relationship difficulties, etc.
Establish impact
* ‘Has alcohol affected your mental health?’ (psychiatric impact)
* ‘Has alcohol affected your medical health?’ Ask about alcohol-related disorders, e.g. liver disease, cardiovascular disease, neurological disorders (physical impact)
* ‘Has alcohol caused any problems with work, relationships or the law?’ (social impact)

92
Q

risk assessment for alcohol abuse

A
  • Suicide and self harm
  • Education about withdrawing e.g. the dangers